Residual Risk Assessment for 7 Source Categories: 

Printing and Publishing 

Marine Tank Vessel Loading Operations 

Pharmaceuticals Production 

Epichlorohydrin Elastomers 

Polybutadiene Rubber 

Styrene Butadiene 

Nitrile Butadiene 

by 

EPA’s Office of Air Quality Planning and Standards 

Office of Air and Radiation 

January 2011 
Table of Contents 

1 Introduction ............................................................................................................................. 5

2 Methods ................................................................................................................................... 6

2.1 Emissions and source data ................................................................................................ 6

2.2 Dispersion modeling for inhalation exposure assessment ................................................ 6

2.3 Estimating human inhalation exposure ............................................................................ 9

2.4 Acute risk screening and refined assessments ................................................................ 10

2.5 Multipathway and environmental risk screening ........................................................... 11

2.6 Dose-response assessment .............................................................................................. 12

2.6.1 Sources of chronic dose-response information ....................................................... 12

2.6.2 Sources of acute dose-response information ........................................................... 21

2.7 Risk characterization ...................................................... Error! Bookmark not defined.

2.7.1 General .................................................................... Error! Bookmark not defined.

2.7.2 Mixtures .................................................................. Error! Bookmark not defined.

2.7.3 Facility-wide risks ................................................... Error! Bookmark not defined.

3 Results summaries and risk characterizations for the 7 source categoriesError! Bookmark not defined.

3.1 Printing and publishing................................................... Error! Bookmark not defined.

3.1.1 Source category description and results .................. Error! Bookmark not defined.

3.1.2 Risk characterization ............................................... Error! Bookmark not defined.

3.2 Marine tank vessel loading ............................................. Error! Bookmark not defined.

3.2.1 Source category description and results .................. Error! Bookmark not defined.

3.2.2 Risk characterization ............................................... Error! Bookmark not defined.

3.3 Pharmaceuticals production ........................................... Error! Bookmark not defined.

3.3.1 Source category description and results .................. Error! Bookmark not defined.

3.3.1 Risk characterization ............................................... Error! Bookmark not defined.

3.4 Epichlorohydrin elastomers production ......................... Error! Bookmark not defined.

3.4.1 Source category description and results .................. Error! Bookmark not defined.

3.4.2 Risk characterization ............................................... Error! Bookmark not defined.

3.5 Polybutadiene rubber production ................................... Error! Bookmark not defined.

3.5.1 Source category description and results .................. Error! Bookmark not defined.

3.5.2 Risk characterization ............................................... Error! Bookmark not defined.

3.6 Styrene butadiene rubber and latex production .............. Error! Bookmark not defined.

3.6.1 Source category description and results .................. Error! Bookmark not defined.

3.6.2 Risk characterization ............................................... Error! Bookmark not defined.

3.7 Nitrile butadiene rubber production ............................... Error! Bookmark not defined.

3.7.1 Source category description and results .................. Error! Bookmark not defined.

3.7.2 Risk characterization ............................................... Error! Bookmark not defined.

4 General discussion of uncertainties and how they have been addressedError! Bookmark not defined.

4.1 Exposure modeling uncertainties ................................... Error! Bookmark not defined.

4.2 Uncertainties in the dose-response relationships ............ Error! Bookmark not defined.

5 References ............................................................................. Error! Bookmark not defined.
Index of Tables 

Table 2.2-1 AERMOD version 09292 model options for RTR II modeling ................................. 7

Table 2.6-1.A Dose-Response Values for Chronic Inhalation Exposure to Carcinogens ........... 17

Table 2.6-2.A Dose-Response Values for Chronic Inhalation Exposure to Noncarcinogens ..... 19

Table 2.6-2.B Dose-Response Values for Chronic Oral Exposure to Noncarcinogens ............... 21

Table 3.1-1 Summary of Emissions and Availability of Dose-Response Values for the 

Printing and Publishing Source Category ..................................... Error! Bookmark not defined.

Table 3.1-2 Summary of Source Category Level Risks for Printing and PublishingError! Bookmark not def

Table 3.1-3 Summary of Acute Refined Results for Printing and PublishingError! Bookmark not defined.

Table 3.1-4 Source Category Contribution to Facility-Wide Cancer Risks – Printing and 

Publishing ...................................................................................... Error! Bookmark not defined.

Table 3.2-1 Summary of Emissions and Availability of Dose-Response Values for the Marine 

Tank Vessel Loading Operations Source Category ...................... Error! Bookmark not defined.

Table 3.2-2 Summary of Source Category Level Risks for Marine Tank Vessel Loading 

Operations ..................................................................................... Error! Bookmark not defined.

Table 3.2-3 Source Category Contribution to Facility-Wide Cancer Risks – Marine Tank 

Vessel ............................................................................................ Error! Bookmark not defined.

Table 3.3-1 Summary of Emissions and Availability of Dose-Response Values for the 

Pharmaceuticals Production Source Category .............................. Error! Bookmark not defined.

Table 3.3-2 Summary of Source Category Level Risks for PharmaceuticalsError! Bookmark not defined.

Table 3.3-3 Summary of Acute Refined Results for Pharmaceuticals ProductionError! Bookmark not defin

Table 3.3-4 Summary Category Contribution to Facility-Wide Cancer Risks - 

Pharmaceuticals ............................................................................ Error! Bookmark not defined.

Table 3.4-1 Summary of Emissions and Availability of Dose-Response Values for the 

Epichlorohydrin Elastomers Production Source Category ........... Error! Bookmark not defined.

Table 3.4-2 Summary of Source Category Level Risks for Epichlorohydrin Elastomers 

Production ..................................................................................... Error! Bookmark not defined.

Table 3.4-3 Source Category Contribution to Facility-Wide Cancer Risks - EpichlorohydrinError! Bookmar

Table 3.5-1 Summary of Emissions and Availability of Dose-Response Values for the 

Polybutadiene Rubber Source Category ....................................... Error! Bookmark not defined.

Table 3.5-2 Summary of Source Category Level Risks for Polybutadiene Rubber ProductionError! Bookma

Table 3.5-2 Source Category Contribution to Facility-Wide Cancer Risks - PolybutadieneError! Bookmark 

Table 3.6-1 Summary of Emissions and Availability of Dose-Response Values for Styrene 

Butadiene Rubber and Latex Production ...................................... Error! Bookmark not defined.

Table 3.6-2 Summary of Source Category Level Risks for Styrene Butadiene – Rubber and 

Latex Production ........................................................................... Error! Bookmark not defined.

Table 3.6-2 Source Category Contribution to Facility-Wide Cancer Risks - StyreneError! Bookmark not de

Table 3.7-1 Summary of Emissions and Availability of Dose-Response Values for Nitrile 

Butadiene Rubber Production ....................................................... Error! Bookmark not defined.

Table 3.7-2 Summary of Source Category Level Risks for Nitrile Butadiene Rubber 

Production ..................................................................................... Error! Bookmark not defined.

Table 3.7-2 Source Category Contribution to Facility-Wide Cancer Risks – Nitrile ButadieneError! Bookma
Appendices 

Appendix 1 Emissions Inventory Support Memorandums 

Appendix 2 Technical Support Document for HEM-AERMOD Modeling 

Appendix 3 Meteorological Data for HEM-AERMOD Modeling 

Appendix 4 Analysis of data on short-term emission rates relative to long-term emission 

rates 

Appendix 5 TRIM-Based Multipathway Screening Scenario 

Appendix 6 Detailed Risk Modeling Results 

Appendix 7 Acute Impacts Refined Analysis Figures 

Index of Acronyms 

AERMOD American Meteorological Society/EPA Regulatory Model 

AEGL Acute exposure guideline level 

ASTDR US Agency for Toxic Substances and Disease Registry 

CalEPA California Environmental Agency 

ERPG Emergency Response Planning Guideline 

HAP Hazardous Air Pollutant 

HEM Human Exposure Model 

HI Hazard index 

HQ Hazard quotient 

IRIS Integrated Risk Information System 

MACT Maximum Achievable Control Technology 

MOA Mode of action 

NATA National Air Toxics Assessment 

NEI National Emissions Inventory 

POM Polycyclic organic matter 

REL Reference exposure level 

RfC Reference concentration 

RfD Reference dose 

TOSHI Target-organ-specific hazard index 

URE Unit risk estimate
1 Introduction 

Section 112 of the Clean Air Act (CAA) establishes a two-stage regulatory process for 

addressing emissions of hazardous air pollutants (HAPs) from stationary sources. In the first 

stage, section 112(d)(2) requires the Environmental Protection Agency (EPA, or the Agency) 

to develop technology-based standards for categories of industrial sources (e.g., petroleum 

refineries, pulp and paper mills, etc.) [1]. EPA has largely completed the initial Maximum 

Achievable Control Technology (MACT) standards as required under this provision. Under 

section 112(d)(6), EPA must review each of these technology-based standards at least every 

eight years and revise a standard, as necessary, “taking into account developments in 

practices, processes and control technologies.” In the second stage, EPA is required under 

section 112(f)(2) to assess the health and environmental risks that remain after 

implementation of the MACT standards. If additional risk reductions are necessary to protect 

public health with an ample margin of safety or to prevent an adverse environmental effect, 

EPA must develop standards to address these remaining risks. This second stage of the 

regulatory process is known as the residual risk stage. For each source category for which 

EPA issued MACT standards, the residual risk stage must be completed within eight years of 

promulgation of the initial technology-based standard. 

In December of 2006 we consulted with a panel from the EPA's Science Advisory Board 

(SAB) on the “Risk and Technology Review (RTR) Assessment Plan” and in June of 2007, 

we received a letter with the results of that consultation. Subsequent to the consultation, in 

July of 2009, a meeting was held with an SAB panel for a formal peer review of the “Risk and 

Technology Review (RTR) Assessment Methodologies” [2]. We received the final SAB 

report on this review in May of 2010 [3]. Where appropriate, we have responded to the key 

messages from this review in developing our current risk assessments and we will be 

continuing our efforts to improve our assessments by incorporating updates based on the SAB 

recommendations as they are developed and become available. Our responses to the key 

recommendations of the SAB are outlined in a memo entitled “EPA’s Actions in Response to 

Key Recommendations of the SAB Review of RTR Risk Assessment Methodologies” [4]. 

This document contains the methods and the results of baseline risk assessments (i.e., after the 

implementation of the respective MACT standard) performed for 7 source categories. The 7 

source categories are: 

 

Printing and Publishing 

Marine Tank Vessel Loading 

Pharmaceuticals Production 

Epichlorohydrin Elastomers 

Polybutadiene Rubber 

Styrene Butadiene 

Nitrile Butadiene
The methods discussion includes descriptions of the methods used to develop refined 

estimates of chronic inhalation exposures and human health risks for both cancer and 

noncancer endpoints, as well as descriptions of the methods used to screen for acute health 

risks, chronic non-inhalation health risks, and adverse environmental effects. Since none of 

the screening assessments indicated any significant potential for chronic non-inhalation health 

effects, or environmental impacts including effects to threatened and endangered species, no 

further refinement of these assessments was performed. Screening assessments indicated a 

concern for acute health effects for all 5 of the source categories. Thus, a more refined 

analysis for acute exposure impacts for 5 source categories was performed. 

2 Methods 

2.1 Emissions and source data 

Data from the 2005 National Emissions Inventory (NEI) which were used and published as 

part of the 2005 National-Scale Air Toxics Assessment (NATA) served as the starting point 

for this assessment. The 2005 NEI contains information on actual emissions during the entire 

2005 base year. Using the process MACT code1

, we developed a subset of this inventory that 

contains emissions and facility data for each of the 3 source categories addressed. Next, we 

performed an engineering review of the information using EPA engineers who were directly 

involved in the development of the MACT standards for these 7 source categories, and/or who 

have extensive knowledge of the characteristics of these industries. NEI data was updated 

with industry supplied data as available. The goal of the engineering review was to identify 

readily-apparent limitations and issues with the emissions data (particularly those that would 

greatly influence risk estimates) and to make changes to the data set where possible to address 

these issues and decrease the uncertainties associated with the assessment. 

Details on the development of the emissions and source data for these source categories are 

discussed in Section 3. The emissions data and modifications made to the NEI data are 

discussed in the Appendix 1, entitled “Emissions Inventory Support Memorandums.” 

2.2 Dispersion modeling for inhalation exposure assessment 

Both long- and short-term inhalation exposure concentrations and associated health risk from 

each facility in each of the source categories of interest were estimated using the Human 

Exposure Model in combination with the American Meteorological Society/EPA Regulatory 

Model dispersion modeling system (HEM-AERMOD). The approach used in applying this 

modeling system is outlined below, and further details are provided in Appendix 2. HEMAERMOD performs three main operations: atmospheric dispersion modeling, estimation of 

individual human exposures and health risks, and estimation of population risks. This section 

focuses on the dispersion modeling component. The exposure and risk characterization 

components are discussed in other subsections of sections 2 and 3. 

 

1

 The tagging of data with MACT codes allows EPA to determine reductions attributable to the MACT program. 

The NEI associates MACT codes corresponding to MACT source categories with stationary major and area 

source data. MACT codes may be assigned either at the process level or at the site level in the point source data 

(e.g., the MACT code for municipal waste combustors (MWCs) is assigned at the site level whereas the MACT 

code for petroleum refinery catalytic cracking is assigned at the process level). 
The dispersion model in the HEM-AERMOD system, AERMOD version 09292, is a state-ofthe-science Gaussian plume dispersion model that is preferred by EPA for modeling point, 

area, and volume sources of continuous air emissions from facility applications [5]. Further 

details on AERMOD can be found in the AERMOD Users Guide [6]. The model is used to 

develop annual average ambient concentration through the simulation of hour-by-hour 

dispersion from the emission sources into the surrounding atmosphere. Hourly emission rates 

used for this simulation are generated by evenly dividing the total annual emission rate from 

the inventory into the 8,760 hours of the year. 

The first step in the application of the HEM-AERMOD modeling system is to predict ambient 

concentrations at locations of interest. The AERMOD model options employed are 

summarized in Table 2.2-1 and are discussed further below. 

Table 2.2-1 AERMOD version 09292 model options for RTR II modeling 

Modeling Option Selected Parameter for chronic exposure 

Type of calculations Hourly Ambient Concentration 

Source type Point, area represented as pseudo point source 

Receptor orientation Polar (13 rings at 16 radials) 

Discrete (census block centroids) 

Terrain characterization Actual from USGS 1-degree DEM data 

Building downwash Not Included 

Plume deposition/depletion Not Included 

Urban source option No 

Meteorology 1 year representative NWS from nearest site (158 stations) 

 In HEM-AERMOD, meteorological data are ordinarily selected from a list of 158 National 

Weather Service (NWS) surface observation stations across the continental United States, 

Alaska, Hawaii, and Puerto Rico. In most cases the nearest station is selected as 

representative of the conditions at the subject facility. Ideally, when considering off-site 

meteorological data most site specific dispersion modeling efforts will employ up to five 

years of data to capture variability in weather patterns from year to year. However, because 

we had insufficient number of appropriately formatted model input files derived from 

available meteorological data, we modeled only a single year, typically 1991. While the 

selection of a single year may result in under-prediction of long-term ambient levels at some 

locations, likewise it may result in over-prediction at others. For each facility identified by its 

characteristic latitude and longitude coordinates, the closest meteorological station was used 

in the dispersion modeling. The average distance between a modeled facility and the 

applicable meteorological station was 40 miles (72 km). Appendix 3 (Meteorological Data 

Processing Using AERMET for HEM-AERMOD) provides a complete listing of stations and 

assumptions along with further details used in processing the data through AERMET. The 
sensitivity of model results to the selection of the nearest weather station and the use of one 

year of meteorological data is discussed in “Risk and Technology Review (RTR) Risk 

Assessment Methodologies” [2]. 

The HEM-AERMOD system estimates ambient concentrations at the geographic centroids of 

census blocks (using the 2000 Census), and at other receptor locations that can be specified by 

the user. The model accounts for the effects of multiple facilities when estimating 

concentration impacts at each block centroid. Typically we combined only the impacts of 

facilities within the same source category, and assessed chronic exposure and risk only for 

census blocks with at least one resident (i.e., locations where people may reasonably be 

assumed to reside rather than receptor points at the fenceline of a facility). Chronic ambient 

concentrations were calculated as the annual average of all estimated short-term (one-hour) 

concentrations at each block centroid. Possible future residential use of currently uninhabited 

areas was not considered. Census blocks, the finest resolution available in the census data, 

are typically comprised of approximately 40 people or about ten households. 

In contrast to the development of ambient concentrations for evaluating long-term exposures, 

which was performed only for occupied census blocks, worst-case short-term (one-hour) 

concentrations were estimated both at the census block centroids and at points nearer the 

facility that represent locations where people may be present for short periods, but generally 

no nearer than 100 meters from the center of the facility (note that for large facilities, this 

100-meter ring could still contain locations inside the facility property). Since short-term 

emission rates were needed to screen for the potential for hazard via acute exposures, and 

since the NEI contains only annual emission totals, we applied the general assumption to all 

source categories that the maximum one-hour emission rate from any source was ten times the 

average annual hourly emission rate for that source. 

The average hourly emissions rate is defined as the total emissions for a year divided by the 

total number of operating hours in the year. This choice of a factor of ten for screening was 

originally based on engineering judgment. To develop a more robust peak-to-mean emissions 

factor, and in response to one of the key messages from the SAB consultation on our RTR 

Assessment Plan, we performed an analysis using a short-term emissions dataset from a 

number of sources located in Texas (originally reported on by Allen et al. 2004)[7]. In that 

report, the Texas Environmental Research Consortium Project compared hourly and annual 

emissions data for volatile organic compounds for all facilities in a heavily-industrialized 4-

county area (Harris, Galveston, Chambers, and Brazoria Counties, TX) over an eleven-month 

time period in 2001. We obtained the dataset and performed our own analysis, focusing that 

analysis on sources which reported emitting high quantities of HAP over short periods of time 

(see Appendix 4, “Analysis of data on short-term emission rates relative to long-term 

emission rates”). Most peak emission events were less than twice the annual average, the 

highest was a factor of 74 times the annual average, and the 99th percentile ratio of peak 

hourly emission rate to the annual hourly emission rate was 9. Based on these results, we 

chose the factor of ten for all initial screening; it is intended to cover routinely-variable 

emissions as well as startup, shutdown, and malfunction (SSM) emissions. While there are 

some documented emission excursions above this level, our analysis of the data from the 

Texas Environmental Research Consortium suggests that this factor should cover more than 
99% of the short-term peak gaseous or volatile HAP emissions from typical industrial 

sources. 

 

Census block elevations for HEM-AERMOD modeling were determined nationally from the 

US Geological Service 1-degree digital elevation model (DEM) data files, which have a 

spatial resolution of about 90 meters. Elevations of polar grid points used in estimating shortand long-term ambient concentrations were assumed to be equal to the highest elevation of 

any census block falling within the polar grid sector corresponding to the grid point. If a 

sector does not contain any blocks, the model defaults to the elevation to that of the nearest 

block. If the elevation is not provided for the emission source, the model takes the average 

elevation of all sectors of the nearest model ring. 

In addition to using receptor elevation to determine plume height, AERMOD adjusts the 

plume’s flow if nearby elevated hills are expected to influence the wind patterns. For details 

on how hill heights were estimated and used in the AERMOD modeling see Appendix 2. 

2.3 Estimating human inhalation exposure 

We used the annual average ambient air concentration of each HAP at each census block 

centroid as a surrogate for the lifetime inhalation exposure concentration of all the people who 

reside in the census block. That is, this risk analysis did not consider either the short-term or 

long-term behavior (mobility) of the exposed populations and its potential influence on their 

exposure. 

 

We did not address short-term human activity for two reasons. First, our experience with the 

1996, 1999, 2002, and 2005 NATA assessments (which modeled daily activity using EPA’s 

HAPEM model ) suggests that, given our current understanding of microenvironment 

concentrations and daily activities, modeling short-term activity would, on average, reduce 

risk estimates about 25% for particulate HAPs; it will also reduce risk estimates for gaseous 

HAPs, but typically by much less. Second, basing exposure estimates on average ambient 

concentrations at census block centroids may underestimate or overestimate actual exposure 

concentrations at some residences. Further reducing exposure estimates for the most highlyexposed residents by modeling their short-term behavior could add a systematic low bias to 

these results. 

We did not address long-term migration nor population growth or decrease over 70 years, 

instead basing the assessment on the assumption that each person’s predicted exposure is 

constant over the course of their lifetime which is assumed to be 70 years. In assessing cancer 

risk, we generally estimated three metrics; the maximum individual risk (MIR) which is 

defined as the risk associated with a lifetime of exposure at the highest concentration, the 

population risk distribution, and the cancer incidence. This assumption of not considering 

short or long-term population mobility does not bias the estimate of the theoretical MIR nor 

does it affect the estimate of cancer incidence since the total population number remains the 

same. It does, however, affect the shape of the distribution of individual risks across the 

affected population, shifting it toward higher estimated individual risks at the upper end and 
reducing the number of people estimated to be at lower risks, thereby biasing the risk 

estimates high. 

When screening for potentially significant acute exposures, we used an estimate of the highest 

hourly ambient concentration at any off-site location as the surrogate for the maximum 

potential acute exposure concentration for any individual. 

2.4 Acute risk screening and refined assessments 

In establishing a scientifically defensible approach for the assessment of potential health risks 

due to acute exposures to HAP, we followed the same general approach that has been used for 

developing chronic health risk assessments under the residual risk program. That is, we 

developed a tiered, iterative approach. This approach to risk assessment was endorsed by the 

National Academy of Sciences in its 1993 publication “Science and Judgment in Risk 

Assessment” and subsequently was adopted in the EPA’s “Residual Risk Report to Congress” 

in 1999. 

The assessment methodology is designed to eliminate from further consideration those 

facilities for which we have confidence that no acute adverse health effects of concern will 

occur. To do so, we use what is called a tiered, iterative approach to the assessment. This 

means that we began with a screening assessment, which relies on readily available data and 

uses conservative assumptions that in combination approximate a worst-case exposure. The 

result of this screening process is that either the facility being assessed poses no acute health 

risks (i.e., it “screens out”), or that it requires further, more refined assessment. A refined 

assessment could use industry- or site-specific data on the temporal pattern of emissions, the 

layout of emission points at the facility, the boundaries of the facility, and/or the local 

meteorology. In some cases, all of these site-specific data would be needed to refine the 

assessment; in others, lesser amounts of site-specific data could be used to determine that 

acute exposures are not a concern, and significant additional data collection would not be 

necessary. 

Acute health risk screening was performed as the first step. We used conservative 

assumptions for emission rates, meteorology, and exposure location. We used the following 

worst-case assumptions in our screening approach: 

• Peak 1-hour emissions were assumed to equal 10 times the average 1-hour emission 

rates. 

• For facilities with multiple emission points, peak 1-hour emissions were assumed to 

occur at all emission points at the same time. 

• For facilities with multiple emission points, 1-hour concentrations at each receptor 

were assumed to be the sum of the maximum concentrations due to each emission 

point, regardless of whether those maximum concentrations occurred during the same 

hour. 

• Worst-case meteorology (from one year of local meteorology) was assumed to occur 

at the same time the peak emission rates occur. The recommended EPA local-scale 

dispersion model, AERMOD, is used for simulating atmospheric dispersion. 
• A person was assumed to be located downwind at the point of maximum impact 

during this same 1-hour period, but no nearer to the source than 100 meters. 

• The maximum impact was compared to multiple short-term health benchmarks for the 

chemical being assessed to determine if a possible acute health risk might exist. These 

benchmarks are described in section 2.6 of this report. 

As mentioned above, when we identify acute impacts which exceed their relevant 

benchmarks, we pursue refining our acute screening estimates. In some cases, this includes 

use of a refined emissions multiplier to estimate the peak hourly emission rates from the 

average rates. For the source categories in the document, we conducted a review of the layout 

of emission points at the facilities with the facility boundaries to determine the maximum offsite acute impact for the facilities that did not screen out during the initial model run. Refer to 

Appendix 7 for the detailed results for these sites. 

2.5 Multipathway and environmental risk screening 

The potential for significant human health risks due to exposures via routes other than 

inhalation (i.e., multipathway exposures) or adverse environmental impacts were screened by 

first determining whether any sources emitted any hazardous air pollutants known to be 

persistent and bioaccumulative in the environment (PB-HAP). The PB-HAP compounds or 

compound classes are identified for the screening from the EPA’s Air Toxics Risk 

Assessment Library [8]. Examples of PB-HAP are cadmium compounds, chlordane, 

chlorinated dibenzodioxins and furans, DDE, heptachlor, hexachlorobenzene, 

hexachlorocyclohexane, lead compounds, mercury compounds, methoxychlor, 

polychlorinated biphenyls, polycyclic organic matter (POM), toxaphene, and trifluralin. 

Emissions of POM, lead, cadmium, and mercury were identified in the emissions inventory 

for the source categories included in this document. 

These emissions were evaluated for potential non-inhalation risks and adverse environmental 

impacts using our recently-developed screening scenario which was developed for use with 

the TRIM.FaTE2 model. This screening scenario uses environmental media outputs from the 

peer-reviewed TRIM.FaTE to estimate the maximum potential ingestion risks for any 

specified emission scenario by using a generic farming/fishing exposure scenario that 

simulates a subsistence environment. The screening scenario retains many of the ingestion 

and scenario inputs developed for EPA’s Human Health Risk Assessment Protocols 

(HHRAP) for hazardous waste combustion facilities.3

 In the development of the screening 

scenario a sensitivity analysis was conducted to ensure that its key design parameters were 

established such that environmental media concentrations were not underestimated, and to 

also minimize the occurrence of false positives for human health endpoints. See Appendix 5 

for a complete discussion of the development and testing of the screening scenario, as well as 

for the values of facility-level de minimis emission rates developed for screening potentially 

significant multi-pathway impacts. For the purpose of developing de minimis emission rates 

 

2

 EPA’s Total Risk Integrated Methodology (General Information) http://epa.gov/ttn/fera/trim_gen.html 3

 EPA’s Human Health Risk Assessment Protocol (HHRAP) for Hazardous Waste Combustion Facilities; 

http://www.epa.gov/epaoswer/hazwaste/combust/riskvol.htm#volume1 
for our multi-pathway screening, we derived emission levels for each PB HAP at which the 

maximum human health risk would be 1 in a million for lifetime cancer risk or a hazard 

quotient of 1.0 for noncancer impacts. In evaluating the potential multi-pathway risks from 

emissions of lead compounds, rather than developing a de minimis emission rate, we 

compared maximum estimated chronic (3-month average) atmospheric concentrations with 

the current National Ambient Air Quality Standard (NAAQS) for lead. Values below the 

NAAQS were considered to have a low potential for multi-pathway risks of any significance. 

In all instances, modeling of emissions of cadmium, mercury, and POM associated with the 7 

source categories using our screening scenario indicated that human exposures via noninhalation pathways were well below levels of concern for cancer risk or noncancer hazard. 

For the purposes of this screening assessment, the levels of concern below which risks were 

considered insignificant were 1 in a million for lifetime cancer risk and a hazard quotient of 

1.0 for noncancer impacts. In evaluating emissions of lead compounds, since an ingestion 

reference dose has not been established for chronic noncancer effects, we compared 

maximum chronic atmospheric concentrations with the current National Ambient Air Quality 

Standard (NAAQS) for lead (0.15 ug/m3) and noted that all impacts are well below this value, 

allowing us to conclude that potential multipathway risks from lead compounds are 

insignificant. 

Additionally, we evaluated the potential for significant ecological exposures to non PB-HAP 

from exceedances of chronic human health inhalation thresholds in the ambient air near these 

facilities. Human health dose-response threshold values are generally derived from studies 

conducted on laboratory animals (such as rodents) and developed with the inclusions of 

uncertainty factors that could be as high as 3000. As a result, these human threshold values 

are often significantly lower than the level expected to cause an adverse effect in an exposed 

rodent. It should be noted that there is a scarcity of data on the direct atmospheric impact of 

these HAPs on other receptors, such as plants, birds, and wildlife. Thus, if the maximum 

inhalation hazard in an ecosystem is below the level of concern for humans, we have 

generally concluded that mammalian receptors should be at no risk of adverse effects due to 

inhalation exposures from non PB-HAP, and have assured that other ecological receptors are 

also not at any significant risk from direct atmospheric impact. In some isolated cases where 

we have data indicating potential adverse impacts on plants, birds, or other wildlife due to the 

direct atmospheric impacts of specific HAPs, we note that as an uncertainty and, where 

possible, refine our analysis by comparing our modeled impacts to available threshold values 

from the scientific literature. 

2.6 Dose-response assessment 

2.6.1 Sources of chronic dose-response information 

Dose-response assessment information (carcinogenic and non-carcinogenic) for chronic 

exposure (either by inhalation or ingestion) for the HAPs reported in the emissions inventory 

were based on the EPA Office of Air Quality Planning and Standards’ existing 

recommendations for HAPs [9], also used for NATA 1999, 2002, and 2005 [10]. This 

information has been obtained from various sources and prioritized according to (1) 

conceptual consistency with EPA risk assessment guidelines and (2) level of peer review 
received. The prioritization process was aimed at incorporating into our assessments the best 

available science with respect to dose-response information. The recommendations are based 

on the following sources, in order of priority: 

1) US Environmental Protection Agency (EPA). EPA has developed dose-response 

assessments for chronic exposure for many of the pollutants in this risk assessment. These 

assessments typically provide a qualitative statement regarding the strength of scientific 

data and specify a reference concentration (RfC, for inhalation) or reference dose (RfD, 

for ingestion) to protect against effects other than cancer and/or a unit risk estimate (URE, 

for inhalation) or slope factor (SF, for ingestion) to estimate the probability of developing 

cancer. The RfC is defined as “an estimate (with uncertainty spanning perhaps an order of 

magnitude) of a continuous inhalation exposure to the human population (including 

sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects 

during a lifetime”. The RfD is “an estimate (with uncertainty spanning perhaps an order 

of magnitude) of a daily oral exposure to the human population (including sensitive 

subgroups) that is likely to be without an appreciable risk of deleterious effects during a 

lifetime.” The URE is defined as “the upper-bound excess cancer risk estimated to result 

from continuous lifetime exposure to an agent at a concentration of 1 μg/m3

 in air.” The 

SF is “an upper bound, approximating a 95% confidence limit, on the increased cancer 

risk from a lifetime exposure to an agent. This estimate, [is] usually expressed in units of 

proportion (of a population) affected per mg/kg-day...” EPA disseminates dose-response 

assessment information in several forms, based on the level of review. The Integrated 

Risk Information System (IRIS) [11] is an EPA database that contains scientific health 

assessment information, including dose-response information. All IRIS assessments since 

1996 have also undergone independent external peer review. The current IRIS process 

includes review by EPA scientists, interagency reviewers from other federal agencies, and 

the public, and peer review by independent scientists external to EPA. New IRIS values 

are developed and old IRIS values are updated as new health effects data become 

available. Refer to the “IRIS Track” website for detailed information on status and 

scheduling of current individual IRIS assessments and updates 

(http://cfpub.epa.gov/ncea/iristrac/index.cfm). EPA’s science policy approach, under the current 

carcinogen guidelines, is to use linear low-dose extrapolation as a default option for 

carcinogens for which the mode of action (MOA) has not been identified. We expect 

future EPA dose-response assessments to identify nonlinear MOAs where appropriate, 

and we will use those analyses (once they are peer reviewed) in our risk assessments. At 

this time, however, there are no available carcinogen dose-response assessments for 

inhalation exposure that are based on a nonlinear MOA. 

2) US Agency for Toxic Substances and Disease Registry (ATSDR). ATSDR, which is part 

of the US Department of Health and Human Services, develops and publishes Minimum 

Risk Levels (MRLs) [12] for inhalation and oral exposure to many toxic substances. As 

stated on the ATSDR web site: “Following discussions with scientists within the 

Department of Health and Human Services (HHS) and the EPA, ATSDR chose to adopt a 

practice similar to that of the EPA's Reference Dose (RfD) and Reference Concentration 

(RfC) for deriving substance specific health guidance levels for non neoplastic endpoints.” 

The MRL is defined as “an estimate of daily human exposure to a substance that is likely 
to be without an appreciable risk of adverse effects (other than cancer) over a specified 

duration of exposure”. ATSDR describes MRLs as substance-specific estimates to be 

used by health assessors to select environmental contaminants for further evaluation. 

Exposures above an MRL do not necessarily represent a threat, and MRLs are therefore 

not intended for use as predictors of adverse health effects or for setting cleanup levels. 

3) California Environmental Protection Agency (CalEPA). The CalEPA Office of 

Environmental Health Hazard Assessment has developed dose-response assessments for 

many substances, based both on carcinogenicity and health effects other than cancer. The 

process for developing these assessments is similar to that used by EPA to develop IRIS 

values and incorporates significant external scientific peer review. As cited in the 

CalEPA Technical Support Document for developing their chronic assessments4: “The 

guidelines for developing chronic inhalation exposure levels incorporate many 

recommendations of the U.S. EPA [13] and NAS [14].” The non-cancer information 

includes available inhalation health risk guidance values expressed as chronic inhalation 

reference exposure levels (RELs) [15]. CalEPA defines the REL as “the concentration 

level at or below which no adverse health effects are anticipated in the general human 

population.” CalEPA's quantitative dose-response information on carcinogenicity by 

inhalation exposure is expressed in terms of the URE [16], defined similarly to EPA's 

URE. 

In developing chronic risk estimates, we adjusted dose-response values for some HAPs based 

on professional judgment, as follows: 

1) In the case of HAP categories such as glycol ethers and cyanide compounds, the most 

conservative dose-response value of the chemical category is used as a surrogate for other 

compounds in the group for which dose-response values were not available. This is done 

in order to examine, under conservative assumptions, whether these HAPs that lack doseresponse values may pose an unacceptable risk and require further examination, or screen 

from further assessment. 

2) Where possible for emissions of unspecified mixtures of HAP categories such as metal 

compounds and POM, we applied category-specific chemical speciation profiles 

appropriate to the source category to develop a composite dose-response value for the 

category. 

3) In 2004, EPA determined that the CIIT dose-response value for formaldehyde (5.5 x 10-9

per μg/m3) was based on better science than the IRIS dose-response value (1.3 x 10-5 per 

μg/m3

), and we switched from using the IRIS value to the CIIT value in risk assessments 

supporting regulatory actions. This determination was based on a substantial body of 

research on the inhalation dosimetry for formaldehyde in rodents and primates by the CIIT 

Centers for Health Research (formerly the CIIT), with a focus on use of rodent data for 

 

4

 Air Toxics Hot Spots Program, Risk Assessment Guidelines, Part III - Technical Support Document 

for the Determination of Noncancer Chronic Reference Exposure Levels. Air Toxicology and Epidemiology 

Section, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency. 

February 2000 (http://www.oehha.ca.gov/air/chronic_rels/pdf/relsP32k.pdf) 
refinement of the quantitative cancer dose-response assessment [17, 18, 19]. The CIIT’s 

risk assessment of formaldehyde incorporated mechanistic and dosimetric information on 

formaldehyde. However, recent research published by EPA indicates that, when the 

CIIT’s two-stage modeling assumptions are varied, resulting dose-response estimates can 

vary by several orders of magnitude [18, 19, 20, 20]. These findings are not supportive of 

interpreting the CIIT model results as providing a conservative (health-protective) 

estimate of human risk [21]. The recent EPA research also examined the contribution of 

the two-stage modeling for formaldehyde towards characterizing the relative weights of 

key events in the mode-of-action of a carcinogen. For example, in the EPA research, the 

model-based inference in the published CIIT study that formaldehyde’s direct mutagenic 

action is not relevant to the compound’s tumorigenicity was found not to hold under 

variations of modeling assumptions [22]. Additionally, in 2007, the California 

Environmental Protection Agency considered a petition to use the CIIT URE value rather 

than its 1992 cancer risk value of 6 X 10-6 per ug/m3

. After consideration and consultation 

with their Scientific Review Panel of Toxic Air Contaminants, they decided not to change 

from their 1992 value [23, 24]. As a result of these findings, EPA no longer considers the 

CIIT URE value to be health protective, and we are again using the Agency’s current 

value on IRIS, which was last revised in 1991, and which is more than 2000 times greater 

than the CIIT value. We note that a new IRIS re-assessment has been drafted and sent to 

the NAS for review. The NAS review is expected to be completed by March of 2011. 

4) The IRIS URE for nickel inhalation was derived from evidence of the carcinogenic effects 

of insoluble nickel compounds in crystalline form. Soluble nickel species, and insoluble 

species in amorphous form, do not appear to produce genotoxic effects by the same toxic 

mode of action as insoluble crystalline nickel. Nickel speciation information for some of 

the largest nickel-emitting sources (including oil combustion, coal combustion, and 

others) suggests that at least 35% of total nickel emissions may be soluble compounds. 

The remaining insoluble nickel emissions are not well-characterized. Consistent with this 

limited information, this assessment will conservatively assume that 65% of emitted 

nickel is insoluble and that all insoluble nickel is crystalline. The nickel URE (based on 

nickel subsulfide, and representative of pure insoluble crystalline nickel) was adjusted to 

reflect an assumption that 65% of the total mass of nickel may be carcinogenic. The 

noncancer dose-response values were not adjusted because noncancer effects of nickel are 

not thought to be limited to the crystalline, insoluble form. 

5) A substantial proportion of POM reported to EPA’s national emission inventory (NEI) 

were not speciated into individual compounds. As a result, it was necessary to apply the 

same simplifying assumptions to this assessment that were used for the 1999 NATA study 

[25]. The NATA approach partitions POM into eight different non-overlapping “groups” 

that were modeled as separate pollutants. Each POM group comprises POM species of 

similar carcinogenic potency, for which we can apply the same URE. 

6) For 2 carcinogenic substances, (isophorone and propylene dichloride) that lack 

inhalation assessments from the sources evaluated in this document, oral 

carcinogenic potency estimates were converted to inhalation UREs. The 

conversion from oral risk (per mg/kg/d oral intake) to inhalation risk (per μg/m3
inhaled) was based on EPA’s standard assumptions of a 70-kg body mass and 20 

m3

/d inhalation rate, as follows:

Where: URE = Unit risk estimate for inhalation (risk per μg/m3

) 

CPS = Carcinogenic potency slope for ingestion (risk per mg oral 

intake per kg body mass per day) 

 EPA understands that conversion of oral dose-response information to inhalation 

exposure may add significant uncertainty to the resulting risk estimates. However, 

the alternative to this would have been to omit these substances from quantitative 

inhalation risk estimates altogether, thereby making a de facto assumption of zero 

carcinogenic potency. For the purposes of the residual risk assessment, EPA 

prefers to use the approach described above to screen these carcinogens for their 

potential contributions to risk. If a substance is determined to be a potentially 

important contributor to risk, it will be prioritized for further dose-response 

development through EPA’s IRIS process. 

The emissions inventories for the 7 source categories include emissions of 85 HAP. Of these, 

34 are classified as known, probable, or possible carcinogens, with quantitative cancer doseresponse values available. These 34 HAP, their quantitative inhalation chronic cancer doseresponse values, and the source of each value are listed in Table 2.6-1.A. The POM 

compounds with chronic oral cancer dose-response values available (for which multipathway 

screening assessments were performed) are listed in Table 2.6-1.B. 

The emissions inventories for the 7 source categories include emissions of 75 HAP with 

quantitative inhalation chronic noncancer threshold values available; two of these HAP 

(cadmium and mercury), for which multipathway assessments were performed, also have 

quantitative oral chronic noncancer threshold values available. These 75 HAP, their threshold 

values, and the source of the value are listed in Table 2.6-2.A and Table 2.6-2.B. 

( ) ⎟

⎟

⎠

⎞

⎜

⎜

⎝

⎛

×⎟

⎟

⎠

⎞

⎜

⎜

⎝

⎛

× × ⎟

⎟

⎠

⎞

⎜

⎜

⎝

⎛

⋅ ⎟ = ⎠

⎞ ⎜

⎝

⎛ − −

g

mg

d

m

kg d kg

mg CPS

m

g URE

μ

μ

1000

1 20

70

1 3 1 1

3
Table 2.6-1.A Dose-Response Values for Chronic Inhalation Exposure to Carcinogens 

URE (unit risk estimate for cancer) = cancer risk per μg/m3 of average lifetime exposure. Sources: IRIS 

= EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Health 

Hazard Assessment, EPA/OAQPS = interim value recommended by the EPA Office of Air Quality 

Planning and Standards, Conv. Oral = Converted from an oral dose-response assessment. 

Pollutant 

CAS 

Number5

URE 

(1/μg/m3) Source 

1,3-Butadiene 106990 3.0E-05 IRIS

1,4-Dioxane 123911 7.7E-06 CAL

2-Nitropropane 79469 5.6E-06 EPA OAQPS

2,4-Toluene diisocyanate 584849 1.1E-05 CAL

Acetaldehyde 75070 2.2E-06 IRIS

Acetamide 60355 2.0E-05 CAL

Acrylonitrile 107131 6.8E-05 IRIS

Allyl chloride 107051 6.0E-06 CAL

Aniline 62533 1.6E-06 CAL

Arsenic compounds 7440382 4.3E-03 IRIS

Benzene 6 71432 7.8E-06 IRIS

Beryllium compounds 7440417 2.4E-03 IRIS

Bis(2-ethylhexyl)phthalate 117817 2.4E-06 CAL

Cadmium compounds 7440439 1.8E-03 IRIS

Carbon tetrachloride 56235 6.0E-6 IRIS

Chromium (VI) compounds 18540299 1.2E-02 IRIS

Epichlorohydrin 106898 1.2E-06 IRIS

Ethyl benzene 100414 2.5E-06 CAL

Ethylene dichloride 107062 2.6E-05 IRIS

Ethylene oxide 75218 8.8E-05 CAL

Formaldehyde 50000 1.3E-05 IRIS

Hydrazine 302012 4.9E-03 IRIS

Isophorone 78591 2.7E-07 Conv. Oral 7

Methyl tert-butyl ether 1634044 2.6E-07 CAL

Methylene chloride 75092 4.7E-07 IRIS

Naphthalene 91203 3.4E-05 CAL

Nickel compounds 7440020 1.6E-04 EPA OAQPS8

p-Dichlorobenzene 106467 1.1E-05 CAL

Polycyclic organic matter (POM) 246 11 EPA OAQPS11

 - Benzo(a)anthracene 56553 1.0E-04 EPA OAQPS9

 

5

 Chemical Abstract Services identification number. For groups of compounds that lack a CAS number we have 

used a surrogate 3-digit identifier corresponding to the group’s position on the CAA list of HAPs. 6

 The EPA IRIS assessment for benzene provides a range of plausible UREs. This assessment used the highest 

value in that range, 7.8E-06 per μg/m3

. The low end of the range is 2.2E-06 per μg/m3. 7

 No inhalation unit risk estimates were available for this compound. Therefore we converted from an IRIS oral 

potency slope of 0.00095 per mg/kg/d. UREs that are converted from the oral route to the inhalation route of 

exposure are considered highly uncertain, and are only used in cases where no other URE is available. 8

 65% of the IRIS URE for nickel refinery dust, as explained above. 
Table 2.6-1.A Dose-Response Values for Chronic Inhalation Exposure to Carcinogens 

URE (unit risk estimate for cancer) = cancer risk per μg/m3 of average lifetime exposure. Sources: IRIS 

= EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Health 

Hazard Assessment, EPA/OAQPS = interim value recommended by the EPA Office of Air Quality 

Planning and Standards, Conv. Oral = Converted from an oral dose-response assessment. 

Pollutant 

CAS 

Number5

URE 

(1/μg/m3) Source 

 - Benzo(a)pyrene 50328 1.0E-03 EPA OAQPS11

 - Benzo(b)fluoranthene 205992 1.0E-04 EPA OAQPS11

 - Benzo(k)fluoranthene 207089 1.0E-04 EPA OAQPS11

 - Chrysene 218019 1.0E-05 EPA OAQPS11

 - Dibenz(a,h)anthracene 53703 1.0E-03 EPA OAQPS11

 - Indeno(1,2,3-cd)pyrene 193395 1.0E-04 EPA OAQPS11

Propylene dichloride 78875 1.9E-05 Conv. Oral 10

Propylene oxide 75569 3.7E-06 IRIS

Tetrachloroethylene 127184 5.9E-06 CAL

Trichloroethylene 79016 2.0E-06 CAL

Vinyl chloride 75014 8.8E-06 IRIS

Table 2.6-1.B Dose-Response Values for Chronic Oral Exposure to Carcinogens 

SF (oral slope factor for cancer) = cancer risk per mg/kg/d of average lifetime exposure. Sources: IRIS 

= EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Health 

Hazard Assessment, EPA/OAQPS = interim value recommended by the EPA Office of Air Quality 

Planning and Standards. 

Pollutant 

CAS 

Number11

SF 

(1/mg/kg/d) Source 

Polycyclic organic matter (POM)12 246 0.5 EPA OAQPS

- Benzo(a)anthracene 56553 1 EPA OAQPS

- Benzo(a)pyrene 50328 10 EPA OAQPS

- Benzo(b)fluoranthene 205992 1 EPA OAQPS

- Benzo(k)fluoranthene 207089 1 EPA OAQPS

- Chrysene 218019 0.1 EPA OAQPS

- Dibenz(a,h)anthracene 53703 10 EPA OAQPS

- Indeno(1,2,3-cd)pyrene 193395 1 EPA OAQPS

 9

 Assigned the URE associated with a mixture of POM compounds having a similar potency. Details of this 

method, also used in the 1999 National Air Toxics Assessment, are available at 

http://www.epa.gov/ttn/atw/nata1999/99pdfs/pomapproachjan.pdf 10 No inhalation unit risk estimates were available for this compound. Therefore we converted from a oral 

potency slope of 0.068 per mg/kg/d. UREs that are converted from the oral route to the inhalation route of 

exposure are considered highly uncertain, and are only used in cases where no other URE is available. 11 Chemical Abstract Services identification number. For groups of compounds that lack a CAS number we 

have used a surrogate 3-digit identifier corresponding to the group’s position on the CAA list of HAPs. 

12 Includes other unspeciated POM emissions (e.g., total PAH). 
Table 2.6-2.A Dose-Response Values for Chronic Inhalation Exposure to 

Noncarcinogens 

RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps 

an order of magnitude) of a continuous inhalation exposure to the human population 

(including sensitive subgroups) that is likely to be without an appreciable risk of deleterious 

effects during a lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL = 

California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency 

for Toxic Substances and Disease Registry. 

Pollutant 

CAS 

Number 

RfC 

(mg/m3) Source 13

1,1,1-Trichloroethane 71556 5 IRIS 

1,2-Epoxybutane 106887 0.02 IRIS -- M 

1,2,4-Trichlorobenzene 120821 0.2 HEAST 

1,3-Butadiene 106990 0.002 IRIS -- M 

1,4-Dioxane 123911 3.6 ATSDR 

2-Nitropropane 79469 0.02 IRIS 

2,4-Toluene diisocyanate 584849 0.00007 IRIS -- M 

Acetaldehyde 75070 0.009 IRIS -- L 

Acetonitrile 75058 0.06 IRIS -- M 

Acrolein 107028 0.00002 IRIS -- M 

Acrylic acid 79107 0.001 IRIS -- M 

Acrylonitrile 107131 0.002 IRIS -- M 

Allyl chloride 107051 0.001 IRIS -- L 

Aniline 62533 0.001 IRIS 

Arsenic compounds 7440382 0.000015 CAL 

Benzene 71432 0.03 IRIS -- M 

Beryllium compounds 7440417 0.00002 IRIS -- M 

Bis(2-ethylhexyl)phthalate 117817 0.01 CAL 

Cadmium compounds 7440439 0.00001 ATSDR 

Carbon disulfide 75150 0.7 IRIS -- M 

Carbon tetrachloride 56235 0.1 IRIS 

Chlorine 7782505 0.00015 ATSDR 

Chlorobenzene 108907 1 CAL 

Chloroform 67663 0.098 ATSDR 

Chromium compounds14 7440473 0.0001 

 - Chromium (VI) compounds 18540299 0.0001 IRIS -- M 

Cobalt compounds 7440484 0.0001 ATSDR 

Cresols (mixed) 1319773 0.6 CAL 

Cumene 98828 0.4 IRIS -- M 

Cyanide compounds15 57125 0.003 IRIS -- L 

Diethanolamine 111422 0.003 CAL 

Dimethyl formamide 68122 0.03 IRIS -- M 

 

13 The descriptors L (low), M (medium), and H (high) have been added for IRIS RfC values to indicate the 

overall level of confidence in the RfC value, as reported in the IRIS file. 

14 Chromium compounds are converted to Chromium (VI) compounds by source category specific ratio. 

15 The value for hydrogen cyanide used as a surrogate. 
Table 2.6-2.A Dose-Response Values for Chronic Inhalation Exposure to 

Noncarcinogens 

RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps 

an order of magnitude) of a continuous inhalation exposure to the human population 

(including sensitive subgroups) that is likely to be without an appreciable risk of deleterious 

effects during a lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL = 

California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency 

for Toxic Substances and Disease Registry. 

Pollutant 

CAS 

Number 

RfC 

(mg/m3) Source 13

Epichlorohydrin 106898 0.001 IRIS -- M 

Ethyl benzene 100414 1 IRIS -- L 

Ethylene dichloride 107062 2.4 ATSDR 

Ethylene glycol 107211 0.4 CAL 

Ethylene oxide 75218 0.03 CAL 

Formaldehyde 50000 0.0098 ATSDR 

Glycol ethers18 171 0.02 IRIS -- M 

 - 2-Butoxyethyl acetate16 112072 0.02 IRIS -- M 

 - Ethylene glycol ethyl ether 110805 0.2 IRIS -- M 

 - Ethylene glycol methyl ether 109864 0.02 IRIS -- M 

 - Diethylene glycol monobutyl ether18 112345 0.02 IRIS -- M 

 - n-Hexyl carbitol18 112594 0.02 IRIS -- M 

Hydrazine 302012 0.0002 CAL 

Hydrochloric acid 7647010 0.02 IRIS -- L 

Hydrofluoric acid 7664393 0.014 CAL 

Hydrogen cyanide 74908 0.003 IRIS -- L 

Isophorone 78591 2 CAL 

Lead compounds 7439921 0.00015 EPA OAQPS 

Manganese compounds 7439965 0.00005 IRIS -- M 

Mercury (elemental) 7439976 0.0003 IRIS -- M 

Methanol 67561 4 CAL 

Methyl chloride 74873 0.09 IRIS -- M 

Methyl isobutyl ketone 108101 3 IRIS -- L/M 

Methyl methacrylate 80626 0.7 IRIS -- M/H 

Methyl tert-butyl ether 1634044 3 IRIS -- M 

Methylene chloride 75092 1 ATSDR 

Methylene diphenyl diisocyanate 101688 0.0006 IRIS -- M 

Naphthalene 91203 0.003 IRIS -- M 

n-Hexane 110543 0.7 IRIS -- M 

Nickel compounds 7440020 0.00009 ATSDR 

p-Dichlorobenzene 106467 0.8 IRIS -- M 

Phenol 108952 0.2 CAL 

Phosgene 75445 0.0003 IRIS -- M 

Phthalic anhydride 85449 0.02 CAL 

Propylene dichloride 78875 0.004 IRIS -- M 

Propylene oxide 75569 0.03 IRIS -- M 

 

16 The value for ethylene glycol methyl ether was used as a surrogate. 
Table 2.6-2.A Dose-Response Values for Chronic Inhalation Exposure to 

Noncarcinogens 

RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps 

an order of magnitude) of a continuous inhalation exposure to the human population 

(including sensitive subgroups) that is likely to be without an appreciable risk of deleterious 

effects during a lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL = 

California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency 

for Toxic Substances and Disease Registry. 

Pollutant 

CAS 

Number 

RfC 

(mg/m3) Source 13

Selenium compounds 7782492 0.02 CAL 

Styrene 100425 1 IRIS -- M 

Tetrachloroethene 127184 0.27 ATSDR 

Toluene 108883 5 IRIS -- H 

Trichloroethylene 79016 0.6 CAL 

Triethylamine 121448 0.007 IRIS -- L 

Vinyl acetate 108054 0.2 IRIS -- H 

Vinyl chloride 75014 0.1 IRIS -- M 

Vinylidene chloride 75354 0.2 IRIS -- M 

Xylenes (mixed)19 1330207 0.1 IRIS -- M 

 - m-Xylene17 108383 0.1 IRIS -- M 

 - o-Xylene19 95476 0.1 IRIS -- M 

 - p-Xylene19 106423 0.1 IRIS -- M 

Table 2.6-3.B Dose-Response Values for Chronic Oral Exposure to Noncarcinogens 

RfD (reference dose) = an estimate (with uncertainty spanning perhaps an order of 

magnitude) of a continuous oral exposure to the human population (including sensitive 

subgroups) that is likely to be without an appreciable risk of deleterious effects during a 

lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL = California EPA 

Office of Environmental Human Health Assessment, ATSDR = US Agency for Toxic 

Substances and Disease Registry. 

Pollutant CAS Number 

RfD 

(mg/kg/d) Source 18

Cadmium compounds 7440439 0.0005 IRIS – H 

Mercuric chloride19 7439976 0.0003 IRIS – H 

 - Methyl mercury21 22967926 0.0001 IRIS – H 

2.6.2 Sources of acute dose-response information 

Hazard identification and dose-response assessment information for preliminary acute 

inhalation exposure assessments are based on the existing recommendations of OAQPS for 

HAPs [26]. Depending on availability, the results from screening acute assessments are 

 

17 The RfC for mixed xylenes was used as a surrogate. 

18 The descriptors L (low), M (medium), and H (high) have been added for IRIS RfC values to indicate the 

overall level of confidence in the RfC value, as reported in the IRIS file. 

19 The multipathway exposure assessment for mercury included fate and transport analysis, that included 

separate oral exposure estimates for divalent mercury and methylmercury. 
compared to both “no effects” reference levels for the general public, such as the California 

Reference Exposure Levels (RELs), as well as emergency response levels, such as Acute 

Exposure Guideline Levels (AEGLs) and Emergency Response Planning Guidelines 

(ERPGs), with the recognition that the ultimate interpretation of any potential risks associated 

with an estimated exceedance of a particular reference level depends on the definition of that 

level and any limitations expressed therein. Comparisons among different available 

inhalation health effect reference values (both acute and chronic) for selected HAPs can be 

found in a newly releasedan EPA document (Reference: U.S. EPA. Graphical Arrays of 

Chemical-Specific Health Effect Reference Values for Inhalation Exposures [Final Report]. 

(U.S. Environmental Protection Agency, Washington, D.C., EPA/600/R-09/061, 2009. 

http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=211003.) 

California Acute Reference Exposure Levels (RELs). The California Environmental 

Protection Agency (CalEPA) has developed acute dose-response reference values for many 

substances, expressing the results as Acute inhalation Reference Exposure Levels (RELs). 

The acute REL (http://www.oehha.ca.gov/air/pdf/acuterel.pdf) is defined by CalEPA as 

“the concentration level at or below which no adverse health effects are anticipated for a 

specified exposure duration [27]. RELs are based on the most sensitive, relevant, adverse 

health effect reported in the medical and toxicological literature. RELs are designed to 

protect the most sensitive individuals in the population by the inclusion of margins of 

safety. Since margins of safety are incorporated to address data gaps and uncertainties, 

exceeding the REL does not automatically indicate an adverse health impact.” Acute 

RELs are developed for 1-hour (and 8-hour) exposures. The values incorporate 

uncertainty factors similar to those used in deriving EPA’s Inhalation Reference 

Concentrations (RfCs) for chronic exposures (and, in fact, California also has developed 

chronic RELs). 

 Acute Exposure Guideline Levels (AEGLs). AEGLs are developed by the National 

Advisory Committee (NAC) on Acute Exposure Guideline Levels (NAC/AEGL) for 

Hazardous Substances, and then reviewed and published by the National Research Council 

As described in the Committee’s “Standing Operating Procedures (SOP)” 

(http://www.epa.gov/opptintr/aegl/pubs/sop.pdf), AEGLs “represent threshold exposure limits 

for the general public and are applicable to emergency exposures ranging from 10 min to 8 h.” 

Their intended application is “for conducting risk assessments to aid in the development of 

emergency preparedness and prevention plans, as well as real time emergency response 

actions, for accidental chemical releases at fixed facilities and from transport carriers.” The 

document states that “the primary purpose of the AEGL program and the NAC/AEGL 

Committee is to develop guideline levels for once-in-a-lifetime, short-term exposures to 

airborne concentrations of acutely toxic, high-priority chemicals.” In detailing the intended 

application of AEGL values, the document states that, “It is anticipated that the AEGL values 

will be used for regulatory and nonregulatory purposes by U.S. Federal and State agencies, 

and possibly the international community in conjunction with chemical emergency response, 

planning, and prevention programs. More specifically, the AEGL values will be used for 

conducting various risk assessments to aid in the development of emergency preparedness and 

prevention plans, as well as real-time emergency response actions, for accidental chemical 

releases at fixed facilities and from transport carriers.” 
 

1. US EPA, 2006. Emission Standards for Hazardous Air Pollutants. 

http://www.epa.gov/ttn/atw/mactfnlalph.html. 

2 US EPA, 2009. Risk and Technology Review (RTR) Risk Assessment Methodologies: For 

Review by the EPA’s Science Advisory Board with Case Studies – MACT I Petroleum Refining 

Sources and Portland Cement Manufacturing. EPA-452/R-09-006. 

http://www.epa.gov/ttn/atw/rrisk/rtrpg.html. 

3. US EPA, 2010. SAB’s Response to EPA’s RTR Risk Assessment Methodologies. 

http://yosemite.epa.gov/sab/sabproduct.nsf/4AB3966E263D943A8525771F00668381/$File/EP

A-SAB-10-007-unsigned.pdf 

4. US EPA, 2010. Memorandum from Dave Guinnup to the RTR Wood Furniture Docket 

(Docket ID Number EPA-HQ-OAR-2010-0786), entitled, “EPA’s Actions in Response to Key 

Recommendations of the SAB Review of RTR Risk Assessment Methodologies”. 

5. US EPA, 2005. Revision to the Guideline on Air Quality Models: Adoption of a Preferred 

General Purpose (Flat and Complex Terrain) Dispersion Model and Other Revisions; Final 

Rule. 40 CFR Part 51. http://www.epa.gov/EPA-AIR/2005/November/Day-09/a21627.htm

6. US EPA, 2004. Users’ guide for the AMS/EPA regulatory model – AERMOD. EPA-454/B03-001. http://www.epa.gov/scram001/7thconf/aermod/aermodugb.pdf. 

7. Allen, D., C. Murphy, Y. Kimura, W. Vizuete, T. Edgar, H. Jeffries, B.-U. Kim, M. Webster, 

and M. Symons, 2004. Variable industrial VOC emissions and their impact on ozone 

formation in the Houston Galveston Area. Final Report: Texas Environmental Research 

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